Presented antigen from damaged pancreatic β cells activates autoreactive T cells in virus-mediated autoimmune diabetes
J. Clin. Invest. Marc S. Horwitz, et al. 109:79 doi:10.1172/JCI11198 [Go to this article.]

Figure 1
(a) Incidence of diabetes in BDC2.5 mice following poly I:C treatment. BDC Tg mice and nontransgenic littermate controls were treated with 100 μg of poly I:C. Alternatively, BDC Tg mice were infected with 100 pfu of CB4. Mice were monitored twice weekly for blood glucose, and mice with two consecutive values over 300 mg/dl were considered diabetic. Both BDC2.5 mice (n = 12) and their nontransgenic littermates (n = 12) were analyzed and compared with untreated BDC Tg mice (n = 20). (b) Incidence of diabetes in BDC2.5 mice following STZ treatment. BDC Tg mice and nontransgenic littermates were treated with single doses of 0, 40, 80, or 160 mg/kg of STZ. Mice were monitored twice weekly for blood glucose, and mice with two consecutive values over 300 mg/dl were considered diabetic. (c) Incidence of diabetes in NOD/Shi mice following STZ treatment. Twelve-week-old NOD/Shi mice (n = 29) were treated with 80 mg/kg of STZ. Mice were monitored twice weekly for blood glucose, and mice with two consecutive values over 300 mg/dl were considered diabetic. Treated mice were analyzed and compared with untreated NOD/Shi mice (n = 10). Mice from all groups were age matched. Groups from b and c were compared for statistical significance by standard χ-square tests. Of the relevant comparisons, significant differences were observed between STZ-treated (80 mg/kg) BDC mice and STZ-treated (80 mg/kg) NOD mice at both 2 (P < 0.001) and 4 (P < 0.001) weeks after treatment.